![]() ![]() Iatrogenic hypoglycemia is seen frequently, often due to missed glucose checks, changing dextrose needs, and iatrogenic insulin overdose. In fact, exogenous dextrose is usually needed an average of 18 hours after the insulin infusion is stopped. It is important to note that as organ function improves, glucose uptake by other cells will increase, putting the patient at risk for delayed hypoglycemia. The hypoglycemia is expected and can be successfully managed with dextrose infusion, as patients are often in an insulin resistant shock state. Hypoglycemia and hypokalemia are the most frequently seen complications from HDI therapy, and there is no clear association between HDI infusion rate and incidence of hypoglycemia or hypokalemia 7,8. For instance, in a swine model of propranolol toxicity, pigs treated with vasopressors alone died within 20 minutes while those treated with HDI survived for 2-3 hours 6. While the efficacy of HDI has not been established with controlled clinical trials, there is substantial evidence from animal models and human case series. The resulting drop in systemic vascular resistance leads to a hypothetical reflex increase in cardiac output, and the vasodilatory effect may enhance perfusion at the capillary level, reducing the microvascular dysfunction seen with cardiogenic shock. HDI also causes vasodilation via enhancement of endothelial nitric oxide synthase (eNOS) by activating the phosphoinositide 3-kinase (PI3K) pathway. Notably, since this inotropy is not mediated by catecholamines, it is not affected by beta blockade. Insulin acts to switch cell metabolism from fatty acids to carbohydrates, restoring calcium fluxes and improving cardiac contractility. Meanwhile, BB poisoning results in impaired lipolysis, glycogenolysis, and insulin release. CCBs inhibit insulin secretion, because calcium must enter beta-islet cells through L-type calcium channels in order for insulin to be released, resulting in hyperglycemia and alteration of myocardial fatty acid oxidation. Insulin increases cardiac output as a strong inotrope (not a vasopressor, notably) 5. While the molecular mechanisms of HDI are complex and not completely understood, it is important to note that insulin is not a specific antidote to CCB or BB agents. Insulin has been recognized as a positive inotrope since the 1920s, shortly after its isolation from the pancreas 4. High dose insulin therapy - How does it work? ![]() Cardiac output should be assessed with methods such as bedside ultrasonography to determine if hypotension is due to vasodilation for which increased vasopressors are needed, or due to cardiogenic shock for which inotropic agents, high dose insulin, lipid emulsion therapy, or ECMO may be needed. When these therapies fail, a medical toxicologist or poison control center should be consulted to assist with further therapy decisions such as: vasopressors/inotropes, HDI, or lipid emulsion therapy. This trend has continued through 2018, where calcium channel blockers and beta blockers were each listed in the top 10 substances associated with the largest number of fatalities 2.įirst line therapy for beta-blocker and calcium channel blocker overdose involves supportive care with IV fluids, atropine, calcium, and can sometimes include glucagon 3. ![]() In 2016, cardiovascular drugs as a class were the second leading cause of poisoning deaths reported to the National Poison Data System (NPDS), the majority of which were beta-blockers and calcium channel-blockers 1.
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